CLINICAL REVIEWS IN ALLERGY & IMMUNOLOGY临床过敏与免疫学评论
CLINICAL REVIEWS IN ALLERGY & IMMUNOLOGY(英文缩写 CLIN REV ALLERG IMMU),ISSN 1080-0549,eISSN 1559-0267,中文译名:临床过敏与免疫学评论 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 10.817 | Q1 |
| 2022 | 9.100 | Q1 |
| 2023 | 8.400 | Q1 |
| 2024 | 11.300 | Q1 |
| 2025 | 11.500 | Q1 |
CLINICAL REVIEWS IN ALLERGY & IMMUNOLOGY 最新收录文献
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1. Beyond the Index Case: A Practical Framework for Cascade Family Screening in Hereditary Angioedema.
1. 超越指示病例：遗传性血管性水肿级联家庭筛查的实用框架PMID:日期:2026-10-01Hereditary angioedema (HAE) is a genetic disorder characterised by recurrent cutaneous or submucosal oedema. Most cases are caused by pathogenic SERPING1 variants (types I and II), while a smaller subset presents with normal C1-inhibitor (C1-INH) levels and function (HAE-nC1INH). Despite its potentially life-threatening attacks, HAE remains under-diagnosed owing to inconsistent screening practices, low clinical awareness, poor patient acceptance, and resource limitations, resulting in diagnostic delays and preventable morbidity. Although international guidelines recommend family screening to identify at-risk relatives, no standardised protocol exists for its systematic implementation. Cascade family screening offers a structured approach to trace and test all known at-risk relatives across generations. Complementing this strategy, dried blood spot (DBS) assays provide a less invasive, cost-effective alternative to conventional serological testing, with particular utility in resource-limited settings. In this review, we critically appraise current screening methodologies, synthesise emerging evidence on cascade family screening and DBS-based diagnostics, and propose an actionable clinical flowchart to standardise identification, testing, and patient education from index case detection through multi-generational family screening.
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2. Rethinking Monospecific Antibody Therapy in Chronic Rhinosinusitis with Nasal Polyps: Dual- and Multispecific Antibodies.
2. 重新思考慢性鼻窦炎伴鼻息肉中的单特异性抗体治疗：双特异性和多特异性抗体PMID:日期:2026-10-01Chronic rhinosinusitis with nasal polyps (CRSwNP) is a heterogeneous inflammatory disorder in which type 2 inflammation predominates but varies in its local organization, clinical context, and downstream tissue effects. Biologics targeting interleukin-4 receptor alpha, immunoglobulin E, the interleukin-5/interleukin-5 receptor axis, and thymic stromal lymphopoietin have expanded treatment options for severe disease and can improve polyp burden, nasal obstruction, olfactory function, quality of life, and corticosteroid- or surgery-related outcomes. However, responses remain variable across patients and clinical domains, and incomplete control may reflect target mismatch, persistent parallel inflammatory pathways, comorbid airway disease, or established tissue remodeling rather than insufficient pathway coverage alone. In this review, we summarize the mechanisms and clinical evidence for current monospecific antibodies and examine biological contexts that may contribute to variable treatment responses, including local IgE activity, microbial and antigenic amplification, nonsteroidal anti-inflammatory drug-exacerbated respiratory disease (N-ERD), comorbid asthma, and persistent epithelial remodeling. We then discuss biomarkers, multidimensional response assessment, and clinical positioning of biologic therapy before evaluating the rationale, boundaries, molecular design, and current pipeline of dual- and multispecific antibodies. Attention is given to whether broader pathway targeting can provide incremental benefit over optimized monospecific therapy, while maintaining acceptable long-term safety, treatment practicality, and economic value. The future role of multispecific biologics in CRSwNP will depend on rational target pairing, comparative clinical evidence, and improved identification of patients most likely to benefit.
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3. Different Inflammatory Phenotypes and Immune Endotypes Drive Disease Heterogeneity in Asthma and COPD.
3. 不同炎症表型和免疫内型驱动哮喘与COPD的疾病异质性PMID:日期:2026-09-24Asthma and chronic obstructive pulmonary disease (COPD) are highly heterogeneous airway disorders that cannot be adequately understood or managed as single disease entities. Instead, both encompass a wide spectrum of inflammatory phenotypes and immune endotypes that differ in pathobiological mechanisms, clinical presentation, exacerbation risk, and therapeutic responsiveness. In asthma, the classical type 2-high eosinophilic phenotype is typically driven by T helper 2 (Th2) cells, group 2 innate lymphoid cells (ILCs), and the canonical cytokines interleukin (IL)-4, IL-5, and IL-13, whereas non-type 2 asthma includes neutrophilic, mixed granulocytic, and paucigranulocytic patterns associated with Th17-related inflammation, epithelial dysfunction, and relative corticosteroid resistance. In COPD, neutrophil-dominant inflammation mediated by macrophages, Th1/Tc1 cells, and, in some patients, Th17-associated pathways has long been considered the dominant immunopathological pattern. However, growing evidence indicates that a substantial subset of patients with COPD exhibit eosinophil-associated, type 2-skewed inflammation with important implications for inhaled corticosteroid responsiveness and biologic therapy. In this review, we distinguish the concepts of phenotype and endotype, summarize the major inflammatory and immune subtypes of asthma and COPD, and discuss their underlying cellular and molecular mechanisms. We further examine clinically relevant biomarkers, including blood and sputum eosinophils, IgE, and fractional exhaled nitric oxide (FeNO), as well as the expanding therapeutic landscape encompassing anti-IgE, anti-IL-5, anti-IL-4Rα, anti-thymic stromal lymphopoietin (anti-TSLP), macrolides, phosphodiesterase-4 inhibitors, and emerging endotype-directed strategies. By comparing asthma and COPD within a unified immunological framework, this review highlights both shared and disease-specific mechanisms of heterogeneity and argues that mechanistically informed phenotyping and endotyping are central to advancing precision medicine in chronic airway disease.
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4. Computational Approaches to Penicillin Allergy De-labelling: A Clinical Review.
4. 青霉素过敏去标签的计算方法：临床综述PMID:日期:2026-09-22Penicillin allergy is recorded in roughly one in ten hospital patients, yet fewer than one in ten of those records reflects a real, clinically significant allergy. The mismatch matters: patients with a penicillin label receive more second-line and broader-spectrum antibiotics, with measurable downstream costs in infection, surgical site morbidity, length of stay, and antimicrobial resistance. Specialist-led skin testing and graded oral challenge remain the diagnostic standard, but the global allergy workforce cannot test the population that needs testing. Validated decision rules such as PEN-FAST, structured non-allergist pathways, and direct oral challenge in low-risk patients have closed part of that gap, but uptake is still limited by inconsistent free-text documentation, variable clinician confidence, and weak integration with electronic health records. This review summarises how computational methods are being added to that pathway. Supervised machine-learning models can mine electronic health records to identify candidates for review. Natural language processing can recover the timing, character, and severity of a reaction from clinic letters that the structured allergy field omitted. Predictive models that combine clinical, laboratory, and immunological inputs are starting to outperform rule-based scores on beta-lactam risk. Decision-support systems are moving past simple drug-name matching toward context-aware alerts. Image classifiers and large language models are opening a route to rapid, photograph-and-history triage. We discuss what is needed for any of this to be safe in routine care: representative training data, transparent model behaviour, regulatory alignment, and prospective evaluation against the outcomes the antimicrobial stewardship community already measures.
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5. Tissue-Resident Macrophages: Linking Physiology and Inflammation in Infection.
PMID:日期:2026-09-11Macrophages are found in every tissue in the body, and their importance goes far beyond clearing pathogens. Developmental studies have shown that many macrophage populations originate during embryogenesis, persist through self-renewal, and adopt transcriptional and functional programs defined by their tissue environment. These tissue-resident macrophages (TRMs) are embedded within organ physiology, where they regulate, for instance, cardiac conduction, sculpt synaptic circuits, recycle iron, maintain epithelial barriers, and coordinate repair. During infection, TRMs connect to neural, metabolic, and structural circuits; therefore, inflammatory activation can alter organ function long after pathogen clearance. We propose that TRMs function as physiological integrators of immunity, translating local environmental cues into immune responses constrained by the demands of their tissue. This review examines macrophage populations across interconnected physiological systems, including the heart-brain axis, the spleen-liver network, and barrier tissues. In these settings, developmental origin, niche-derived signals, and metabolic programming determine how macrophages respond to infection and whether they preserve or disrupt tissue homeostasis. Additionally, we discuss how loss of resident identity during inflammatory stress contributes to chronic pathology and post-infectious sequelae and how emerging therapeutic strategies aim to restore tissue-specific macrophage programs. By framing immunity within organ physiology, we offer a conceptual model for understanding how infection reshapes tissue function through resident macrophages, as well as how targeting these cells could prevent long-term damage.
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6. Targeting IL-33 and TSLP: A Novel Approach to Modulate Type 2 and Non-Type 2 Inflammatory Pathways in Pemphigus Vulgaris.
6. 靶向IL-33和TSLP：一种调控寻常型天疱疮中2型和非2型炎症通路的新方法PMID:日期:2026-09-11Pemphigus vulgaris (PV) is an autoantibody-mediated blistering disorder in which pathogenic immunoglobulins target epidermal desmoglein proteins, leading to suprabasal acantholysis that manifests clinically as flaccid blisters and mucosal erosions. First-line management typically includes oral corticosteroids as well as B-cell-depleting therapies such as rituximab; however, these and other systemic immunosuppressants carry substantial toxicities and are not suitable for all patients, motivating the search for more targeted, well-tolerated alternatives. Although PV is fundamentally driven by anti-desmoglein autoantibodies, emerging evidence implicates type 2 inflammation as a secondary contributor to disease activity, and epithelial-derived cytokines interleukin (IL)-33 and thymic stromal lymphopoietin (TSLP) have garnered interest as upstream modulators of this axis. Beyond canonical type 2 effects, IL-33 and TSLP can influence a broader inflammatory milieu, including modulating type 17 responses that may also contribute to PV immunopathology. No clinical evidence currently supports IL-33 or TSLP blockade in PV, and it remains to be determined if modulation of this secondary axis could potentially control disease as monotherapy. Nonetheless, given their upstream position in cutaneous immune processes, therapeutic blockade of IL-33 or TSLP warrants investigation in preclinical models and biomarker-informed trials, principally as an adjunct to current autoantibody-directed regimens.
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7. Gram-Positive and Gram-Negative Probiotic Extracellular Vesicles: Mechanisms of Immune Modulation and Therapeutic Opportunities in Atopic Dermatitis.
7. 革兰氏阳性与革兰氏阴性益生菌胞外囊泡：免疫调节机制及在特应性皮炎中的治疗机遇PMID:日期:2026-09-11Atopic dermatitis (AD) is a prevalent chronic inflammatory skin disease characterized by epidermal barrier dysfunction, type 2 immune skewing, and microbiome dysbiosis. Although live probiotics can modulate the gut-skin axis, their clinical use is limited by variable efficacy and safety concerns. Probiotic extracellular vesicles (PEVs) have emerged as cell-free nanotherapeutics that retain microbial bioactivity while circumventing the risks associated with live bacteria. However, the comparative immunological roles of vesicles from Gram-positive and Gram-negative probiotics remain incompletely understood. This review systematically compares Gram-negative outer membrane vesicles (OMVs) and Gram-positive membrane vesicles (MVs) in the context of AD. OMVs, enriched with lipopolysaccharide (LPS) and other bioactive cargo, mainly signal through toll-like receptor 4 (TLR4) to regulate innate immunity, strengthen antimicrobial defense, and modulate inflammation. In contrast, Gram-positive MVs, containing lipoteichoic acid (LTA), peptidoglycan (PG), proteins, and small RNAs, preferentially activate TLR2-linked pathways that support immune tolerance, regulatory T cell (Treg) responses, and barrier repair. Both PEV classes demonstrate significant potential in preclinical models by attenuating inflammation, improving epithelial integrity, and restoring microbiome balance. Despite this potential, clinical translation requires standardized isolation protocols, scalable manufacturing, rigorous safety testing, and regulatory alignment. Advances in microbial engineering and EV design may enable targeted, microbiota-directed therapies for AD.
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8. Molecular Signature and miRNA Pattern of CD4 + T Lymphocytes in Plaque Psoriasis.
8. 斑块型银屑病中CD4+ T淋巴细胞的分子特征及miRNA表达模式PMID:日期:2026-09-10Psoriasis is a global health problem affecting approximately 3% of the population. Because this autoimmune and autoinflammatory disease significantly reduces the quality of life and carries the risk of serious complications and comorbidities, all efforts have been directed towards developing effective therapeutic strategies that allow for a significant restoration of immunological homeostasis. To make this possible, basic research is being conducted, among others, to discover the molecular basis responsible for the pathogenic activation of autoreactive lymphocytes. At the same time, microRNAs seem to be very interesting candidates for epigenetic modulation of signaling pathways disturbed in psoriasis, which are themselves also affected in its pathogenesis. Therefore, our narrative review comprehensively summarizes the current knowledge on the molecular signature and miRNA profile that appear characteristic for psoriasis-related CD4 + T lymphocytes and hypothesizes the effects of microRNA dysregulation based on the results of a contextual functional analysis of selected candidates having the greatest impact on the pathogenesis of psoriasis. Detailed considerations allowed us to uncover the most important signaling pathways and microRNA molecules active in pathogenic CD4 + T lymphocytes that are involved in psoriasis progression, and also suggested other microRNAs that appear to have potential therapeutic activity, with the leading opposing roles of interferon regulatory factor 4, microRNA-155 and microRNA-150.
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9. Epidemic Thunderstorm Asthma in China: A Systematic Review of an Artemisia-Associated Phenotype.
PMID:日期:2026-09-02Epidemic thunderstorm asthma (ETSA) has historically been characterised around grass pollen in temperate Australia and Europe, whereas reports from northern China suggest an Artemisia-associated and potentially recurrent pattern. This systematic review synthesises primary evidence on the epidemiology, allergen profile, clinical features and early-warning systems of ETSA, comparing the Chinese and grass-pollen experiences. Following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 statement, PubMed, Web of Science, the China National Knowledge Infrastructure (CNKI) and Wanfang were searched to 30 June 2026, and reference lists were screened. Two reviewers independently selected studies, extracted data and assessed risk of bias with the Newcastle-Ottawa Scale and the Murad tool; certainty was rated using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach. Because of clinical and methodological heterogeneity, no meta-analysis was performed. Of 436 records identified and 333 screened after de-duplication, 54 primary studies were included (43 international and 11 Chinese, spanning Yulin, Hohhot, Chongqing, Lanzhou and Shenzhen). Three recurring observational patterns were identified. Chinese reports, especially from northern and north-western China, frequently described mugwort (Artemisia) sensitisation rather than ryegrass sensitisation; the proportion without a prior asthma diagnosis was high in both settings (approximately 40% to 60% in China and up to 60% to 78% in Australian and United Kingdom cohorts); and recurrent events were reported at individual Chinese localities. Most Chinese reports used genus-level Artemisia or mugwort sensitisation and did not identify the airborne pollen to species. Evidence for direct Artemisia pollen rupture, pollution-related severity modification and pre-emptive treatment was low or very low. Priority research includes field aerosol sampling, prospective validation of locally calibrated warning systems, and trials of pre-emptive inhaled therapy.
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10. Impacts of Environmental Pollutants on Innate Immunity: The Role of Group 2 Innate Lymphoid Cells.
10. 环境污染物对先天免疫的影响：2型先天淋巴细胞的作用PMID:日期:2026-08-29Environmental pollution has emerged as one of the biggest threats to health in the contemporary world. Pollutants modify immune responses and may induce immunotoxicity. In this review, we describe the impact of significant environmental pollutants on the innate immune system, including ozone (O), particulate matter (PM), diesel exhaust particles (DEPs) and cigarette smoke (CS), as well as emerging pollutants such as chemical contaminants, nanomaterials, and microplastics, with a particular focus on the regulatory mechanisms of innate lymphoid cells (ILCs). ILCs, tissue-resident lymphocytes without antigen-specific receptors, have been demonstrated to be essential regulators linking environmental detection and immunological responses. Studies indicate that environmental pollutants activate ILCs and alter the immune responses by compromising the epithelial barrier and triggering the release of alarmins, including interleukin (IL)-33, IL-25, and thymic stromal lymphopoietin (TSLP). Among ILCs, group 2 innate lymphoid cells (ILC2s) are highly sensitive to pollutant-induced epithelial signals and play a critical role in type 2 inflammation. Beyond canonical alarmin signaling, accumulating evidence indicates that environmental pollutants regulate ILC2 biology thereby contributing to immune dysregulation and inflammatory diseases. A better understanding of how environmental pollutants regulate ILC2 activation, plasticity, and functional adaptation will facilitate the development of more precise preventive and therapeutic strategies for pollution-associated diseases.